2014
DOI: 10.1016/j.neubiorev.2014.08.002
|View full text |Cite
|
Sign up to set email alerts
|

Emotional consequences of neuropathic pain: Insight from preclinical studies

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

5
110
0
1

Year Published

2015
2015
2021
2021

Publication Types

Select...
7
1

Relationship

0
8

Authors

Journals

citations
Cited by 154 publications
(116 citation statements)
references
References 175 publications
5
110
0
1
Order By: Relevance
“…Early dysfunctions in central nervous system monoamine transmission, specifically noradrenaline, 5-HT and DA might represent an index of the initiation of long-term plasticity that might underlie pain chronicization or sensitization and ultimately precipitate maladaptive consequences responsible for affective disorders (Yalcin et al, 2014). Here we report that, following peripheral nerve injury, discharge rate of 5-HT DRN neurons and burst firing of VTA DA cells are enhanced, when compared with shamoperated animals.…”
Section: Discussionmentioning
confidence: 73%
See 2 more Smart Citations
“…Early dysfunctions in central nervous system monoamine transmission, specifically noradrenaline, 5-HT and DA might represent an index of the initiation of long-term plasticity that might underlie pain chronicization or sensitization and ultimately precipitate maladaptive consequences responsible for affective disorders (Yalcin et al, 2014). Here we report that, following peripheral nerve injury, discharge rate of 5-HT DRN neurons and burst firing of VTA DA cells are enhanced, when compared with shamoperated animals.…”
Section: Discussionmentioning
confidence: 73%
“…Moreover, increased peripheral sensory nerve activity induces multiple transsynaptic modifications that extend to the central nervous system (Baliki et al, 2006;Baron, 2006;Woolf, 2004;Yalcin et al, 2014Yalcin et al, , 2011. Indeed, chronic maladaptive plasticity underlies emotional, affective and cognitive symptoms of neuropathic pain syndrome, i.e.…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Various mechanisms including axonal remodeling, changes in dendritic spines, dendritic atrophy, synaptic plasticity (eg, synaptogenesis, synapse elimination, long-term potentiation/depression, or synapse turnover), changes in cell size, changes in oxygenation, and neural or glial cell genesis have been suggested to contribute to experience-dependent cortical plasticity. [44][45][46][47][48][49][50] Therefore, future studies with different methodology will be necessary to examine which of these potential mechanisms contribute to structural brain changes in COPD.…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, SNI rats exhibited depression-like behavior (increased forced swimming immobility and decreased sucrose preference, a measure of anhedonia) that was long-lasting when compared to sham-operated rats . In fact, as recently reviewed by Yalcin et al (2014), many early studies modeling depressive consequences of chronic pain utilized animal neuropathic pain models, but yielded conflicting results. Of these studies, those that assessed pain-induced depressive behaviors at later times (>3 weeks) following peripheral nerve injury reported development of a depression-related phenotype (Yalcin et al, 2014).…”
Section: Animal Models Of Comorbid Pain and Depressionmentioning
confidence: 99%